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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:3.)
© 2009 American Heart Association, Inc.

Editorials

Carotid Plaque Stabilization and Progression After Stroke or TIA

Renu Virmani; Aloke V. Finn; Frank D. Kolodgie

From CVPath Institute Inc (R.V., F.D.K.), Gaithersburg, Md; and the Department of Medicine (A.V.F.), Emory University School of Medicine, Atlanta, Ga.

Correspondence to Renu Virmani, MD, Medical Director, CVPath Institute Inc, 19 Firstfield Road, Gaithersburg, MD 20878. E-mail rvirmani@cvpath.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Although plaque rupture is the predominant etiology of carotid artery thrombosis, the stages of lesion progression culminating in a cerebral vascular accident with subsequent plaque passivation is poorly understood. Indeed, the previous largest series of carotid plaques removed at surgery by Redgrave et al implicates plaque rupture as dominant lesion morphology in symptomatic lesions.¹ Notwithstanding, removal of even asymptomatic plaques has been shown to reduce the 5-year incidence of stroke and death as reported by the collaborative group Asymptomatic Carotid Surgery Trial, where 3210 patients undergoing carotid endarterectomy for substantial carotid narrowing of >70% were studied.² Taken together these studies exemplify the importance of plaque rupture and thrombosis as the major contributor of embolization in ischemic stroke. Indeed, these studies are highly reminiscent of coronary disease where the main culprit lesion which gives rise to thrombosis is identified as plaque rupture.³ Moreover, although reports in the literature contend that further lesion progression in coronary arteries manifests through repeated ruptures,^4,5 this concept applied to the carotid, as suggested by Wasserman et al,⁶ has never been confirmed in large patient population presenting with stroke or TIAs.

See accompanying article on page 128

In the largest reported series of carotid endarterectomy specimens acquired from patients with durations <30 days to beyond 180 days after presentation, Peeters et al in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology studied the pathophysiology of lesion stabilization after symptomatic stroke.⁷ Of the plaque characteristics measured with time elapse between the most recent event . . . [Full Text of this Article]

Related Article:

Carotid Atherosclerotic Plaques Stabilize After Stroke: Insights Into the Natural Process of Atherosclerotic Plaque Stabilization

W. Peeters, W.E. Hellings, D.P.V. de Kleijn, J.P.P.M. de Vries, F.L. Moll, A. Vink, and G. Pasterkamp
Arterioscler Thromb Vasc Biol 2009 29: 128-133. [Abstract] [Full Text] [PDF]

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